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This highly aggressive cancer affects mostly young children and is uniformly fatal. Genomic studies show that DIPG is driven by somatic mutations to histone H3, either H3.1 or H3.3 variants (\n                    <jats:italic>HIST1H3B\/C<\/jats:italic>\n                    and\n                    <jats:italic>H3F3A<\/jats:italic>\n                    ), altering the epigenetic landscape of primitive oligodendrocyte or astrocyte precursor cells of the pontine region of the brainstem. Lysine\u2010to\u2010methionine point mutations at amino acid 27 (H3K27M) co\u2010occur with alterations in signaling genes, including the receptor tyrosine kinases (PDGFR\/KIT\/VEGFR\/MET\/EGFR), activin A receptor (ACVR1), intracellular kinases (PI3K\/AKT\/mTOR), cyclin\u2010dependent kinases (CDKs1\/4\/6), transcriptional regulators (MYCN), and tumor suppressors (PTEN\/TP53). This cooperation drives gene expression signatures that inhibit cellular differentiation (ID1\/2, Hedgehog) and promotes malignant transformation. Unique to DIPG, is the frequency of co\u2010occurring sets of genomic insults. However, mapping of the oncogenic signaling pathways activated in response to recurring mutations is unresolved. Herein, known oncogenic signal pathways activated in response to recurring somatic mutations and gene amplifications in DIPG are reviewed. Additionally, an important role for high\u2010resolution quantitative proteomics\/phosphoproteomics in the characterization of signaling cascades are highlighted. These regulate the cell cycle, epigenetics and anti\u2010apoptotic processes, information critical for the development of improved treatment strategies for DIPG.\n                  <\/jats:p>","DOI":"10.1002\/pmic.201800479","type":"journal-article","created":{"date-parts":[[2019,7,22]],"date-time":"2019-07-22T07:44:16Z","timestamp":1563781456000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":63,"title":["Signal Transduction in Diffuse Intrinsic Pontine Glioma"],"prefix":"10.1002","volume":"19","author":[{"given":"Ryan J.","family":"Duchatel","sequence":"first","affiliation":[{"name":"Cancer Signalling Research Group School of Biomedical Sciences and Pharmacy Faculty of Health and Medicine University of Newcastle  Callaghan NSW 2308 Australia"},{"name":"Priority Research Centre for Cancer Research Innovation and Translation Hunter Medical Research Institute  Lambton NSW 2305 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